Abstract
 
Vol 49 No. 4: 349-354 [PDF] [Full Text]
 
The effects of oleanolic acid on atherosclerosis in different animal models
 
Hanqiong Luo, Jine Liu, Qiong Ouyang, Chunxiao Xuan, Lanlan Wang, Tingting Li, and Jun Liu*
Jiangsu Key Laboratory of Drug Screening and Jiangsu Key Laboratory of Drug Discovery for Metabolic Disease, China Pharmaceutical University, Nanjing 210009, China
These authors contributed equally to this work.
 

Abstract  In the present study, three animal models, including C57BL/6J mice, low-density lipoprotein receptor knockout (LDLR−/−) mice, and rabbit that mimicked atherosclerosis, were established to investigate the inhibitory effect of oleanolic acid (OA) on atherosclerosis. In rabbit model, serum total cholesterol (TC), triglyceride, low density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C) were measured. Carotid artery lesions were isolated for histological analysis. The red oil O and hematoxylinCeosin staining in liver were examined. The messenger ribonucleicacid (mRNA) levels of PPARγ, AdipoR1, and AdipoR2 related to lipid metabolism were determined. Compared with model group, OA and atorvastatin significantly lowered the levels of TC and LDL-C. The result of red oil O staining showed that OA and atorvastatin had similar effect on reducing the accumulation of lipid. Histological result demonstrated that OA reduced the thickness of intima. AdipoR1 was markedly increased, while AdipoR2 was remarkably decreased in OA group compared with that in the control group of the rabbit model. In LDLR−/− mouse model, lipid parameters in blood and mRNA levels of PPARγ, AdipoR1, and AdipoR2 were measured. It was found that OA exhibited similar effects as atorvastatin including reduced TG, LDL-C, and enhanced HDL-C. Notably, OA elevated the levels of AdipoR1 and PPARγ. At the same time, OA decreased TC and LDL-C in C57BL/6J mice model. Our results in three different animal models all revealed that OA retarded the development of atherosclerosis by influencing serum lipid levels, lipid accumulation in liver and intimal thickening of artery. And the underlying mechanism of OA on atherosclerosis may involve in lipid metabolism genes: PPARγ, AdipoR1, and AdipoR2.

 

Keywords   oleanolic acid, atherosclerosis, animal model

 

Received   2016-12-4  
Accepted  
2017-2-9

 

Funding  This work was supported by a grant from the National Natural Science Foundation of China (No. 81673443).

 

* Correspondence address  Tel/Fax: +86-25-83271142; E-mail: junliu@cpu.edu.cn

 
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